PAROTID SECRETION OF FLUID, AMYLASE AND KALLIKREIN DURING REFLEX STIMULATION UNDER NORMAL CONDITIONS AND AFTER ACUTE ADMINISTRATION OF AUTONOMIC BLOCKING-AGENTS IN MAN

The purpose of this work was to study the effect of graded mechanical and gustatory stimulation on the secretion of the acinar products fluid and amylase and the ductal product kallikrein from the human parotid gland (n = 9). The involvement of parasympathetic and sympathetic nerves in the salivary reflexes was subsequently examined using receptor blocking agents (n = 4). Chewing elevated the secretion of all products as compared to rest (P < 0.013). When increasing the length of the chewing object, secretion of fluid (P < 0.013), but not enzymes, further increased. The shift from mechanical to gustatory stimulation with 0.5% citric acid enhanced significantly the secretion of amylase and kallikrein (P < 0.009), while application of 5.0% citric acid increased the secretion of both acinar products (P < 0.009) more than kallikrein. A differentiated reflex control of salivation both with regard to input and output was thereby indicated. The muscarinic-cholinergic antagonist oxyphencyclimin reduced median fluid secretion between 54 and 76% depending on the stimuli. During citric acid stimulation, but not during chewing, fluid secretion was reduced about 40% by the beta1-adrenergic antagonist metoprolol, and about 20% by the alpha1-adrenergic antagonist prazosin. Median amylase secretion was reduced 30% during chewing and 75% during gustatory stimulation by metoprolol. It was concluded that the masticatory-salivary reflex mainly activated parasympathetic pathways producing saliva of low protein content. The gustatory-salivary reflex activated sympathetic pathways to a higher extent, resulting in saliva with higher protein content. Using this reflex model, kallikrein secretion seemed not to be mediated by any of the tested receptors.